PASG Passage Bio Inc

Nasdaq: PASG © 2024 Passage Bio. All rights reserved. Corporate Presentation September 2024

2 Forward-Looking Statement This presentation includes “forward-looking statements” within the meaning of, and made pursuant to the safe harbor provisions of, the Private Securities Litigation Reform Act of 1995, including, but not limited to: our expectations about timing and execution of anticipated milestones, including the initiation of dosing of FTD-C9orf72 patients, feedback from regulatory of authorities, the progress of clinical studies and the availability of clinical data from such trials; our expectations about our collaborators’ and partners’ ability to execute key initiatives; our ability to receive milestone payments from our partners; our expectations about cash runway; and the ability of our product candidates to treat their respective target CNS disorders. These forward-looking statements may be accompanied by such words as “aim,” “anticipate,” “believe,” “could,” “estimate,” “expect,” “forecast,” “goal,” “intend,” “may,” “might,” “plan,” “potential,” “possible,” “will,” “would,” and other words and terms of similar meaning. These statements involve risks and uncertainties that could cause actual results to differ materially from those reflected in such statements, including: our ability to develop and obtain regulatory approval for our product candidates; the timing and results of preclinical studies and clinical trials; risks associated with clinical trials, including our ability to adequately manage clinical activities, unexpected concerns that may arise from additional data or analysis obtained during clinical trials, regulatory authorities may require additional information or further studies, or may fail to approve or may delay approval of our drug candidates; the occurrence of adverse safety events; the risk that positive results in a preclinical study or clinical trial may not be replicated in subsequent trials or success in early stage clinical trials may not be predictive of results in later stage clinical trials; failure to protect and enforce our intellectual property, and other proprietary rights; our dependence on collaborators and other third parties for the development and manufacture of product candidates and other aspects of our business, which are outside of our full control; risks associated with current and potential delays, work stoppages, or supply chain disruptions; and the other risks and uncertainties that are described in the Risk Factors section in documents the company files from time to time with the Securities and Exchange Commission (SEC), and other reports as filed with the SEC. Passage Bio undertakes no obligation to publicly update any forward-looking statement, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise.

3 REDEFINING THE COURSE OF NEURODEGENERATIVE CONDITIONS Advancing potential best-in-class, one-time progranulin raising FTD-GRN gene therapy In-house manufacturing process development to support program execution Strong cash position with runway expected to the end of 2Q 2026* Exploring benefits of elevated progranulin in multiple adult neurodegenerative diseases * Based on cash, cash equivalents and marketable securities as of June 30, 2024 and initial proceeds from out-licensing of pediatric programs.

4 Validating the Therapeutic Potential of PBFT02 Promising data from initial clinical study of PBFT02 in FTD-GRN Genetic form of FTD caused by GRN mutations, which lead to progranulin (PGRN) deficiency No approved disease-modifying therapies One-time therapy Proprietary AAV1 construct Nonsurgical injection directly to cerebrospinal fluid (CSF) Durable, elevated CSF PGRN levels* Urgent Patient Need in FTD-GRN Differentiated, Potential Best-in-Class Profile Fast Track and Orphan Drug Designation * Based on interim data.

5 Significant Market Opportunity for PBFT02 Across Multiple Neurodegenerative Diseases ~18,000 ~21,000 ~72,600 ~3.9M FTD-GRN1–3 FTD-C9orf722–4 AMYOTROPHIC LATERAL SCLEROSIS (ALS) 5–6 ALZHEIMER’S DISEASE (GRN SNP)*7–8 * rs5848 single nucleotide polymorphism (SNP) 1. Greaves CV, et al. J Neurol 2019; 266:2075-2086. 2. Galvin JE, et al. Neurology 2017; 89:2049-2056. 3. Onyike CU, et al. Int Rev Psychiatry 2013; 25:130-137. 4. Moore KM, et al. Lancet Neurol 2020; 19: 145–156. 5. Brown et al. Neuroepi 2021; 55:342-353. 6. CDC ALS Registry Dashboard. 7. Sheng J, et al. Gene 2014; 141-145. 8. Alz Assoc. 2023 Alzheimer’s Disease Facts and Figures. Alzheimers Dement 2023;19. Estimated Prevalence (US and EU)

6 Anticipated Upcoming Milestones and Data Readouts 2H 2024 1H 2025 2H 2025 Obtain regulatory feedback on the pathway to treating ALS patients Report 12-month Cohort 1 and interim Cohort 2 data FTD-GRN Milestones FTD-C9orf72 and ALS Milestones Initiate dosing of FTD-C9orf72 patients Seek regulatory feedback on pivotal trial design

PBFT02 Frontotemporal Dementia-GRN

8 FTD: A Devastating Adult Disease OVERVIEW • Fatal adult-onset neurodegenerative disease affecting the frontal and temporal lobes of the brain, characterized by a decline in behavior, language and executive function • One of the most common causes of early-onset dementia worldwide, disproportionately affecting individuals aged 40-65 years CLINICAL SYMPTOMS Disease progression is rapid and degenerative, including loss of speech, loss of expression, behavioral changes and immobility On average, people with FTD live 8 years after the onset of symptoms

9 Progranulin Deficiency is the Defining Characteristic of FTD-GRN and Leads to Neurodegeneration Progranulin is critical to maintaining CNS cell homeostasis Rhinn H et al. Trends Pharm Sci. 2022, 43:641-652.

10 Elevated PGRN Increases Potential for Improved Cellular Function • Progranulin is a secreted protein that binds to cell membrane receptors to affect multiple intracellular pathways –Major role is regulating intracellular lysosomal activity –Extracellular PGRN is endocytosed via multiple receptors • Driving elevated PGRN levels in the extracellular space increases the amount of PGRN available to enter target CNS cells • Able to leverage cross-correction mechanism: secreted PGRN can be taken up by non-transduced cells Paushter et al., Acta Neuropathol. 2018;136(1):1-17., Rhinn et al., Trends in Pharmacological Sciences 2022; 43.8:641-652.

11 Preclinical: AAV1 Achieved the Highest Levels of CSF PGRN in NHPs AAV1 increased CSF PGRN levels ~5x more than AAV5 and AAVhu68 (proprietary AAV9 variant) vectors, without further elevating peripheral levels Production of Human PGRN in Plasma AAV1 transgene delivery led to highest hPGRN levels in CSF CSF PGRN (ng/mL) 0 10 20 30 40 CSF 0.1 1 10 100 LLOQ Normal Day RA2981 RA2982 RA3027 RA3153 RA3151 RA3170 RA3155 RA3160 AAVhu68 AAVhu68 (v2) AAV1 AAV5 RA2981 RA2982 RA3027 RA3153 RA3151 RA3170 RA3155 RA3160 AAVhu68 AAVhu68 (v2) AAV1 AAV5 RA2981 RA2982 RA3027 RA3153 RA3151 RA3170 RA3155 RA3160 AAVhu68 AAVhu68 (v2) AAV1 AAVhu68 AAV5 AAVhu68 (v2) AAV5 AAV1 Normal LLOQ Plasma Plasma PGRN (ng/mL) 0 10 20 30 40 0.1 1 10 100 Normal Day 1,000 Left, right: Two adult rhesus macaques per treatment received ICM AAV.hPGRN High dose, 3.0 x 1013 GC / 3.3 x 1011 GC/g brain) on study day 01 .. Shading: Reference range for healthy adult controls’ PGRN levels in CSF (n = 61) and plasma (n = 56) (Passage Bio data).

12 Preclinical: ICM Administration of PBFT02 to NHPs Led to Broad Distribution of Vector Throughout Brain/Spinal Cord PBFT02 distribution after ICM administration to NHPs FCX PCX TCX OCX Hip Med CBL Cerv Thor Lum Cerv Thor Lum TRG Brain Spinal Cord DRG PBFT02 • Vector distributed to all sampled areas of brain and spinal cord • 3.0 x 1012 GC NHP dose equivalent to clinical Dose 1 of PBFT02 in upliFT-D study

13 Preclinical: Higher CSF PGRN May Confer Reduction in Inflammatory Response • Microgliosis: inflammatory response to pathogenic insults in the CNS • CD68: marker of activated microglia Thalamus data shown above. Thalamic atrophy is a key feature commonly found in FTD PBFT02 reduced lipofuscin at all doses, suggesting correction of underlying mechanism of disease • Lipofuscin: increased levels associated with lysosomal dysfunction • Correlated with underlying mechanism of FTD-GRN Microgliosis reduction strongest at highest PBFT02 dose / PGRN level Murine FTD Model Murine FTD Model *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, one-way ANOVA followed by Tukey’s multiple comparisons test

14 upliFT-D: Global Phase 1/2 Trial with PBFT02 DURATION 2 years; with additional 3 years of follow-up for safety and durability of effect PRIMARY ENDPOINTS Safety and tolerability SECONDARY ENDPOINTS Biomarkers • Progranulin (CSF, plasma) • GFAP (CSF, plasma) • vMRI • Retinal nerve fiber layer and retinal lipofuscin deposits via OCT • NfL (CSF, plasma) Clinical • CDR + NACC FTLD sum of boxes EXPLORATORY BIOMARKERS • Cathepsin D (CSF) • LAMP 1 (CSF) • Lys-GL1 (CSF) COHORT 1 Dose 1 (3.3e10 GC/g)* COHORT 2 Dose 2 (1.1e11 GC/g)* OPTIONAL COHORT 3 Optional dose 3 Recruiting IDMC review Phase 1/2 Multicenter Open-label Dose escalation study Up to 15 patients across 3 cohorts 1/2 TRIAL DESIGN COHORT 1 (n=5) Dose 1 COHORT 2 (n=3-5) Dose 1 OPTIONAL COHORT 3 IDMC review Phase Multicenter Open-label Dose escalation study Up to 15 patients across 3 cohorts 1/2 Complete Dose 1: 3.3e10 GC/g estimated brain weight.

15 Intra-Cisterna Magna (ICM) Administration • Directly deliver vector into the CSF via a single injection to reach both CNS and peripheral tissues1 –Allows for broad CNS biodistribution –Lower doses compared to IV systemic delivery –Reduced impact of neutralizing antibodies • Brief (<60 min), non-surgical, CT-guided procedure to allow for precise delivery to the cisterna magna –Infusion catheter does not enter brain tissues Cisterna magna 1. Hinderer et. al, Human Gene Therapy. 2018 Jan; 29(1):15-24​.

16 upliFT-D: Interim Data from Cohort 1 Patients • PBFT02 was well-tolerated among the four patients (P2-5) who received revised immunosuppression regimen –Among these patients, there were no SAEs; only mild-to-moderate treatment emergent AEs were reported • No evidence of DRG toxicity, as measured by nerve conduction studies • No complications during ICM administration observed Safety* Efficacy / Target Engagement • Interim data demonstrates PBFT02 potential for best-in-class efficacy at Dose 1 • Relative to baseline, PBFT02 increased CSF PGRN expression in all patients consistently; up to 6-fold at Day 30 (n=5) and up to 10-fold at Day 180 (n=2) • CSF PGRN levels remained elevated at Day 360 (n=1) SAE: serious adverse event; AE: adverse event; DRG: dorsal root ganglion; ICM: intracisterna magna *Patient safety follow-up ranged from 2 to 12 months post-dosing as of data cutoff of August 20, 2024

17 • Potential best-in-class PGRN profile at Dose 1 • Continued elevation of CSF PGRN at 6-months (n=2) and 12-months (n=1) –Patient 2 rate of increase slowed between Day 180 and 360 (D30-180: 58% vs. D180-360: 26%) • Consistent response across all treated patients Initial Patients Treated with PBFT02 Have Seen a Substantial Increase in CSF PGRN Dosing D30 D60 D180 D360 Patient 1 1.9 12.7 N/A N/A N/A Patient 2 2.8 17.3 N/A 27.3 34.2 Patient 3 2.9 10.7 13.7 21.7 Patient 4 2.2 12.3 N/A Patient 5 2.3 13.6 N/A CSF Progranulin (ng/mL) Shading: Reference range for healthy adult controls’ PGRN levels in CSF (range: 3.28 – 8.15 ng/mL, mean: 4.76 ng/mL, n = 61) (Passage Bio data) CSF=Cerebrospinal fluid 0 3 6 9 12 15 18 21 24 27 30 33 36 0 30 60 180 360 CSF PGRN, ng/mL Time (days) Dose 1 Progranulin, CSF Patient 1 Patient 2 Patient 3 Patient 4 Patient 5

18 • Plasma PGRN levels remained below normal levels at up to 12 months post-dose • PGRN increased only in the CSF, where it has potential to correct neurodegeneration Plasma PGRN Levels Remained Below Normal Levels Post-Dose Shading: Lower limit of normal reference range for healthy adult controls’ PGRN levels in plasma (91.6 – 372.4 ng/mL, n = 56) (Passage Bio data) 0 10 20 30 40 50 60 70 80 90 100 0 7 14 30 60 90 180 360 Plasma PGRN, ng/mL Time (days) Dose 1 Progranulin, Plasma Patient 1 Patient 2 Patient 3 Patient 4 Patient 5

19 Summary SAFETY1 PBFT02 Dose 1 generally well-tolerated to date among the four Cohort 1 patients who received revised steroid regimen following protocol amendment • No serious AEs • All AEs mild to moderate in intensity • No evidence of clinically significant immune response, hepatotoxicity or venous sinus thrombosis • No evidence of DRG toxicity • No complications during ICM administration observed BIOMARKERS • Potential best-in-class PGRN profile at Dose 1 • Continued elevation of CSF PGRN at 6-months (n=2) and 12-months (n=1) • Consistent response across Cohort 1 patients (n=5) •No increase in plasma PGRN levels up to 12-months ANTICIPATED NEXT STEPS • Report 12-month Cohort 1 and interim Cohort 2 data in 1H 2025 • Seek regulatory feedback on pivotal trial design in 2H 2025 AEs=adverse events; ICM=intra-cisterna magna; DRG=dorsal root ganglia 1. Patient safety follow-up ranged from 2 to 12 months post-dosing as of data cutoff of August 20, 2024

Looking Ahead

21 PBFT02 has Potential to Correct Underlying Pathology in FTD-GRN, FTD-C9orf72 and ALS TDP-43 pathology is a hallmark of multiple neurodegenerative diseases1 • TDP-43 mislocalizes from nucleus to cytoplasm • Forms inclusion bodies associated with neurodegeneration 1. Rhinn H et al. Trends Pharm Sci. 2022, 43:641-652

22 TDP-43 pathology due to lysosomal dysfunction (GRN/ TMEM106 double knockout, DKO) reduced by AAV.hPGRN1 Elevated PGRN Ameliorates TDP-43 Pathology in Preclinical Models AAV delivered hPGRN to DKO mouse brain TDP-43 pathology in DKO mice reduced by AAV.hPGRN Elevated PGRN reduced insoluble TDP-43 in mouse spinal cord Elevated PGRN extended survival of TDP-43 mutant mice Elevated PGRN ameliorated TDP-43 pathology and disease course in a preclinical model2 • Elevated PGRN also prevented degeneration of large axon fibers in TDP-43 mice • PGRN neuroprotection from pleiotropic effect, not single pathway 1. Reich et al. (2023) bioRxiv preprint 07.14.549089; 2. Beel et al (2018) Mol Neurodegen; Laird et al. (2010) Plos One. DKO=double gene knockout; GRN=granulin gene; PGRN=progranulin; TDP-43=transactive response DNA binding protein 43 kDa. † PGRN increased to >2x endogenous levels

23 GRN rs5848 SNP associated with accelerated disease in FTD-C9orf72 patients Decreased PGRN Associated with Greater Disease Severity in Multiple CNS Conditions GRN rs5848 SNP associated with accelerated disease in FTD-C9orf72 patients 1. van Blitterswijk et al (2014) Mol Neurodegen. AD=Alzheimer’s disease; ALS=amyotrophic lateral sclerosis; GRN=granulin gene; PGRN=progranulin; SNP=single nucleotide polymorphism. PGRN SNPs are genetic risk factors for CNS diseases • GRN rs5848 SNP results in ~15% reduction in PGRN levels • PGRN SNPs increase risk for, and worsen severity of, FTD/ALS-C9orf72 and AD1

24 • GRN SNP rs5848 carriers have reduced PGRN levels and increased risk for AD • AD patients with GRN SNP rs5848 show reduced PGRN levels and increased CSF tau • GRN SNP rs5848 is estimated to occur in 30% of the general population, with a similar prevalence rate among AD patients2 • PGRN ablation exacerbates AD pathology in mice • PGRN overexpression reduces pathology burden in AD models Genetic Risk1 Prevalence Supporting Preclinical Evidence3 PBFT02 has Potential to Modulate Alzheimer’s Disease SNP=single nucleotide polymorphism. Third-party preclinical data. Sources: 1. Chen Y et al. J Neurol. 2015, 262:814-22; Takahashi H et al. Acta Neuropathol. 2017, 133:785-807. 2. Fenoglio C et al. J Alzheimers Dis. 2009, 18:603-612 (allele frequency used to estimate prevalence among AD patients). 3. Hosokawa M et al. J Neuropath Exp Neurol. 2015, 74:158-65; Minami SS et al. Nat Med. 2014, 20:1157-64; Van Kampen JM & Kay DG. PLoS ONE 2017, 12:e0182896.

25 Leading In-House CMC Capabilities to Support PBFT02 Development Proven analytical development capabilities In-House CMC Analytical Capabilities to Support Program Advancement and Future Commercialization of PBFT02 Integrated process development GMP QC capabilities Strong regulatory CMC scientific expertise Scale-up capability

26 Upcoming Milestones and Corporate Updates PIPELINE • Advancing Huntington’s disease preclinical program • Licensed pediatric clinical-stage programs (GM1, Krabbe and MLD) to GEMMA Biotherapeutics BALANCE SHEET • Cash balance of $92 million as of 6/30/24* • Cash runway to the end of 2Q 2026* * Based on cash, cash equivalents and marketable securities and initial proceeds from out-licensing of pediatric programs. TIMING MILESTONE FTD-GRN 1H 2025 Report 12-month Cohort 1 and interim Cohort 2 data 2H 2025 Seek regulatory feedback on pivotal trial design PBFT02 Additional Indications 2H 2024 Obtain regulatory feedback on clinical pathway for treating ALS patients 1H 2025 Initiate dosing of FTD-C9orf72 patients

27 REDEFINING THE COURSE OF NEURODEGENERATIVE CONDITIONS Advancing potential best-in-class, one-time progranulin raising FTD-GRN gene therapy In-house manufacturing process development to support program execution Strong cash position with runway expected to the end of 2Q 2026* Exploring benefits of elevated progranulin in multiple adult neurodegenerative diseases * Based on cash, cash equivalents and marketable securities as of June 30, 2024 and initial proceeds from out-licensing of pediatric programs.

Thank You passagebio.com | NASDAQ: PASG

29 Focused Pipeline Addressing Rare and Prevalent Neurodegenerative Indications Program Indication US/EU prevalence Discovery Preclinical Phase 1/2 Pivotal PBFT02 Frontotemporal dementia - GRN 18,0001-3 Frontotemporal dementia - C9orf72 21,0002-4 Amyotrophic lateral sclerosis 72,6005-6 Alzheimer’s disease with rs5848 SNP 3.9M7-8 Unnamed Huntington’s disease 60,0009 PBGM01 GM1 gangliosidosis PBKR03 Krabbe disease PBML04 Metachromatic leukodystrophy Licensed to GEMMA Biotherapeutics 1. Greaves CV, et al. J Neurol 2019; 266:2075-2086. 2. Galvin JE, et al. Neurology 2017; 89:2049-2056. 3. Onyike CU, et al. Int Rev Psychiatry 2013; 25:130-137. 4. Moore KM, et al. Lancet Neurol 2020; 19: 145–156. 5. Brown et al. Neuroepi 2021; 55:342-353. 6. CDC ALS Registry Dashboard. 7. Sheng J, et al. Gene 2014; 141-145. 8. Alz Assoc. 2023 Alzheimer’s Disease Facts and Figures. Alzheimers Dement 2023;19. 9. Crowell et al. Neuroepi. 2021; 55:361-368

30 Demonstrated Leadership LEADERSHIP TEAM Deep experience in rare disease, CNS disorders and genetic medicines Eden Fucci SVP Technical Operations BOARD OF DIRECTORS Maxine Gowen, Ph.D. Chairwoman Athena Countouriotis, M.D. Avenzo Therapeutics Derrell Porter, M.D. cTRL Therapeutics Dolan Sondhi, Ph.D. Weill Cornell Medicine Sandip Kapadia Harmony Biosciences Saqib Islam, J.D. SpringWorks Thomas Kassberg Ultragenyx William Chou, M.D. President & Chief Executive Officer Stuart Henderson Chief Business Officer William Chou, M.D. President & Chief Executive Officer Chip Cale General Counsel & Corporate Secretary Kathleen Borthwick Chief Financial Officer Karl Whitney SVP Global Regulatory Affairs Sue Browne, Ph.D. Chief Scientific Officer

W&dϬϮ​ǁĂƐ​ǁĞůůͲƚŽůĞƌĂƚĞĚ​ĂŵŽŶŐ​ŽŚŽƌƚ​ϭ​ƉĂƌƟĐŝƉĂŶƚƐ​ǁŚŽ​ƌĞĐĞŝǀĞĚ​ ĞŶŚĂŶĐĞĚ​ŝŵŵƵŶŽƐƵƉƉƌĞƐƐŝŽŶ • dƐ​ǁĞƌĞ​ƌĞƉŽƌƚĞĚ​ŝŶ​Ăůů​ƉĂƌƟĐŝƉĂŶƚƐ​;Ŷсϱͬϱ​΀ϭϬϬ͘Ϭй΁Ϳ͖​ŵŽƐƚ​;ϯϴͬϰϬ​ĞǀĞŶƚƐͿ​ǁĞƌĞ​ ŵŝůĚͲƚŽͲŵŽĚĞƌĂƚĞ͘​Ɛ​ǁĞƌĞ​ƌĞƉŽƌƚĞĚ​ĨŽƌ​ŽŶĞ​ƉĂƌƟĐŝƉĂŶƚ​;Ŷсϭͬϱ​΀ϮϬ͘Ϭй΁Ϳ​;Table 2Ϳ • KŶĞ​ƉĂƌƟĐŝƉĂŶƚ͕​ƚŚĞ​ĮƌƐƚ​ƚƌĞĂƚĞĚ​;Ŷсϭͬϱ​΀ϮϬ͘Ϭй΁Ϳ͕​ŚĂĚ​ƚǁŽ​ƚƌĞĂƚŵĞŶƚͲƌĞůĂƚĞĚ​Ɛ​ ĂŶĚ​ǁŝƚŚĚƌĞǁ​ĨƌŽŵ​ƚŚĞ​ƐƚƵĚLJ​;Table 2Ϳ • dŚĞ​ĮƌƐƚ​ƉĂƌƟĐŝƉĂŶƚ​ƚƌĞĂƚĞĚ​ǁŝƚŚ​W&dϬϮ​ƌĞĐĞŝǀĞĚ​ϲϬ​ŵŐ​ŽƌĂů​ƉƌĞĚŶŝƐŽŶĞ​ĚĂŝůLJ​ƚŚƌŽƵŐŚ​ ϲϬ​ĚĂLJƐ͘​dŚŝƐ​ƉĂƌƟĐŝƉĂŶƚ​ŚĂĚ​ĂŶ​ĂƐLJŵƉƚŽŵĂƟĐ​ĐĞƌĞďƌĂů​ǀĞŶŽƵƐ​ƐŝŶƵƐ​ƚŚƌŽŵďŽƐŝƐ​;sdͿ​ ŽŶ​DZ/​ĂŶĚ​ĚŝƐƉůĂLJĞĚ​ĂŶ​ŝŶĐƌĞĂƐĞ​ŝŶ​>dͬd​ϳ​ĚĂLJƐ​ĂŶĚ​ϳ​ǁĞĞŬƐ​ƉŽƐƚͲƚƌĞĂƚŵĞŶƚ͕​ǁŚŝĐŚ​ ƌĞƐƉŽŶĚĞĚ​ƚŽ​/s​ƐƚĞƌŽŝĚƐ͘​ŝůŝƌƵďŝŶ​ůĞǀĞůƐ​ƌĞŵĂŝŶĞĚ​ŶŽƌŵĂů​ƚŚƌŽƵŐŚŽƵƚ • &Žƌ​ƉĂƌƟĐŝƉĂŶƚƐ​Ϯ​ƚŚƌŽƵŐŚ​ϱ͕​ƚŚĞ​ŝŵŵƵŶŽƐƵƉƉƌĞƐƐŝŽŶ​ƌĞŐŝŵĞŶ​ǁĂƐ​ĂĚũƵƐƚĞĚ​ƚŽ​ ϭ​Ő​ŵĞƚŚLJůƉƌĞĚŶŝƐŽůŽŶĞ​/s​ĚĂŝůLJ​ƚŽ​ĚĂLJ​ϯ͕​ĨŽůůŽǁĞĚ​ďLJ​ŽƌĂů​ƉƌĞĚŶŝƐŽŶĞ​ƚŽ​ĚĂLJ​ϲϬ • &Žƌ​ƉĂƌƟĐŝƉĂŶƚƐ​ƌĞĐĞŝǀŝŶŐ​ƚŚĞ​ĂĚũƵƐƚĞĚ​ŝŵŵƵŶŽƐƵƉƉƌĞƐƐŝŽŶ​ƌĞŐŝŵĞŶ͕​ƚŚĞƌĞ​ǁĞƌĞ​ŶŽ​ ƐƵďƐƚĂŶƟĂů​ŝŶĐƌĞĂƐĞƐ​ŝŶ​ŵĂƌŬĞƌƐ​ŽĨ​ŚĞƉĂƚŽƚŽdžŝĐŝƚLJ​;&ŝŐƵƌĞ​ϯͿ͕​ŶŽ​ĞǀŝĚĞŶĐĞ​ŽĨ​sd​ŽŶ​DZ/͕​ ĂŶĚ​ŶŽ​Ɛ​ƵƉ​ƚŽ​ĚĂLJ​ϯϲϬ Interim Safety and Biomarker Data From upliFT-D Trial of PBFT02 in FTD With GRN Mutations Chavez J,1 Forman M,1 Voss T,1 Triglia P,1 Ni YG,1 Browne SE,1 Quadrini KJ,1 Chou W,1 Ducharme S,2 Irwin DJ,3 Santana I,4 Schulz PE,5 Takada L,6 Tartaglia C,7 de Souza LC8 1 Passage Bio, Inc., Philadelphia, PA, USA; 2 Douglas Mental Health University Institute and Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada; 3 Perelman School of Medicine at the University of Pennsylvania; University of Pennsylvania Health System, Philadelphia, PA, USA; 4 Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal; 5 McGovern Medical School, UTHealth Houston, Houston, TX, USA; 6 Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil; 7 University Health Network and Tanz Centre for Research in Neurodegenerative Diseases, Toronto, Ontario, Canada; 8 Hospital das Clínicas Universidade Federal de Minas Gerais, Belo Horizonte, Brazil ďďƌĞǀŝĂƟŽŶƐ sϭ͕​ĂĚĞŶŽͲĂƐƐŽĐŝĂƚĞĚ​ǀŝƌƵƐ​ϭ͖​>d͕​ĂůĂŶŝŶĞ​ƚƌĂŶƐĂŵŝŶĂƐĞ͖​d͕​ĂƐƉĂƌƚĂƚĞ​ĂŵŝŶŽƚƌĂŶƐĨĞƌĂƐĞ͖​ ďǀ&d͕​ďĞŚĂǀŝŽƌĂů​ǀĂƌŝĂŶƚ​ĨƌŽŶƚŽƚĞŵƉŽƌĂů​ĚĞŵĞŶƚŝĂ͖​Z͕​ůŝŶŝĐĂů​ĞŵĞŶƚŝĂ​ZĂƚŝŶŐ​ĐĂůĞ͖​ &͕​ĐĞƌĞďƌŽƐƉŝŶĂů​ĨůƵŝĚ͖​d͕​ĐŽŵƉƵƚĞƌ​ƚŽŵŽŐƌĂƉŚLJ͖​&d͕​ĨƌŽŶƚŽƚĞŵƉŽƌĂů​ĚĞŵĞŶƚŝĂ͖​&dͲGRN͕​ ĨƌŽŶƚŽƚĞŵƉŽƌĂů​ĚĞŵĞŶƚŝĂ​ǁŝƚŚ​ŐƌĂŶƵůŝŶ​ŵƵƚĂƚŝŽŶ͖​GRN͕​ŐƌĂŶƵůŝŶ͖​/D͕​ŝŶƚƌĂͲĐŝƐƚĞƌŶĂ​ŵĂŐŶĂ͖​ /D͕​/ŶĚĞƉĞŶĚĞŶƚ​ĂƚĂ​DŽŶŝƚŽƌŝŶŐ​ŽŵŵŝƚƚĞĞ͖​/s͕​ŝŶƚƌĂǀĞŶŽƵƐ͖​ůǀWW͕​ůŽŐŽƉĞŶŝĐ​ǀĂƌŝĂŶƚ​ ƉƌŝŵĂƌLJ​ƉƌŽŐƌĞƐƐŝǀĞ​ĂƉŚĂƐŝĂ͖​DZ/͕​ŵĂŐŶĞƚŝĐ​ƌĞƐŽŶĂŶĐĞ​ŝŵĂŐŝŶŐ͖​W͕​ƉĂƌƚŝĐŝƉĂŶƚ͖​W'ZE͕​ƉƌŽŐƌĂŶƵůŝŶ͖​ ƐǀWW͕​ƐĞŵĂŶƚŝĐ​ǀĂƌŝĂŶƚ​ƉƌŝŵĂƌLJ​ƉƌŽŐƌĞƐƐŝǀĞ​ĂƉŚĂƐŝĂ͖​dƐ͕​ƚƌĞĂƚŵĞŶƚͲĞŵĞƌŐĞŶƚ​ĂĚǀĞƌƐĞ​ĞǀĞŶƚƐ͖​ Ɛ͕​ƐĞƌŝŽƵƐ​ĂĚǀĞƌƐĞ​ĞǀĞŶƚƐ͖​K͕​ƐLJƐƚĞŵ​ŽƌŐĂŶ​ĐůĂƐƐ͖​h>E͕​ƵƉƉĞƌ​ůŝŵŝƚ​ŽĨ​ŶŽƌŵĂů͘ ŝƐĐůŽƐƵƌĞƐ :͕​D&͕​ds͕​Wd͕​z'E͕​͕​<:Y͕​ĂŶĚ​t​ĂƌĞ​ĐƵƌƌĞŶƚ​Žƌ​ĨŽƌŵĞƌ​ĞŵƉůŽLJĞĞƐ​ŽĨ​WĂƐƐĂŐĞ​ŝŽ͕​/ŶĐ͘​ WƌĞƐĞŶƚĞĚ​Ăƚ​/&d͕​ĞƉƚĞŵďĞƌ​ϭϵͲϮϮ͕​ϮϬϮϰ͕​ŵƐƚĞƌĚĂŵ͕​dŚĞ​EĞƚŚĞƌůĂŶĚƐ ŽŶƚĂĐƚ͗​ŵĞĚŝŶĨŽΛƉĂƐƐĂŐĞďŝŽ͘ĐŽŵ ĂĐŬŐƌŽƵŶĚ • W&dϬϮ​ŝƐ​Ă​ŶŽŶͲƌĞƉůŝĐĂƟŶŐ​ƌĞĐŽŵďŝŶĂŶƚ​sϭ​ ǀĞĐƚŽƌ͕​ǁŚŝĐŚ​ĐĂƌƌŝĞƐ​Ă​ĐŽĚŽŶͲŽƉƟŵŝnjĞĚ​ƐĞƋƵĞŶĐĞ​ ŽĨ​ƚŚĞ​ŚƵŵĂŶ​GRN​ŐĞŶĞ​ƵŶĚĞƌ​ƚŚĞ​ĐŽŶƚƌŽů​ŽĨ​ƚŚĞ​ ƵďŝƋƵŝƚŽƵƐ​ϳ​ƉƌŽŵŽƚĞƌ​;&ŝŐƵƌĞ​ϭͿ ŽŶĐůƵƐŝŽŶƐ • /D​ĂĚŵŝŶŝƐƚƌĂƟŽŶ​ŽĨ​W&dϬϮ​ƌĞƐƵůƚĞĚ​ŝŶ​Ă​ƌŽďƵƐƚ​ ĂŶĚ​ĚƵƌĂďůĞ​ĞůĞǀĂƟŽŶ​ŽĨ​&​W'ZE​ůĞǀĞůƐ͕​ǁŚŝĐŚ​ǁĂƐ​ ŵĂŝŶƚĂŝŶĞĚ​ƵƉ​ƚŽ​ϭͲLJĞĂƌ​ƉŽƐƚͲƚƌĞĂƚŵĞŶƚ • WůĂƐŵĂ​W'ZE​ůĞǀĞůƐ​ǁĞƌĞ​ŶŽƚ​ŝŵƉĂĐƚĞĚ​ďLJ​W&dϬϮ​ ĂĚŵŝŶŝƐƚƌĂƟŽŶ • /Ŷ​ƚŚĞ​ĨŽƵƌ​ƉĂƌƟĐŝƉĂŶƚƐ​ǁŚŽ​ƌĞĐĞŝǀĞĚ​ƚŚĞ​ƌĞǀŝƐĞĚ​ ŝŵŵƵŶŽƐƵƉƉƌĞƐƐŝŽŶ​ƌĞŐŝŵĞŶ͕​ƚŚĞƌĞ​ǁĞƌĞ​ŶŽ​Ɛ​ĂŶĚ​ ŶŽ​ĞǀŝĚĞŶĐĞ​ŽĨ​ĐůŝŶŝĐĂůůLJ​ƐŝŐŶŝĮĐĂŶƚ​ŝŵŵƵŶĞ​ƌĞƐƉŽŶƐĞ • 'ŝǀĞŶ​ƚŚĞ​ƌŽďƵƐƚ​&​W'ZE​ƌĞƐƉŽŶƐĞ͕​ŽŚŽƌƚ​Ϯ​ǁŝůů​ ĐŽŶƟŶƵĞ​ƚŽ​ĞǀĂůƵĂƚĞ​ŽƐĞ​ϭ ZĞƐƵůƚƐ WĂƌƟĐŝƉĂŶƚ​ϭ​ƌĞĐĞŝǀĞĚ​ƚŚĞ​ŝŶŝƟĂů​ŝŵŵƵŶŽƐƵƉƉƌĞƐƐŝŽŶ​ƌĞŐŝŵĞŶ​ĂŶĚ​ĚŝƐƉůĂLJĞĚ​ŵĂƌŬĞĚůLJ​ŝŶĐƌĞĂƐĞĚ​>dͬd​ůĞǀĞůƐ​;>d​ϭϲdž​h>E͖​d​ϰdž​h>EͿ​ ĨŽůůŽǁŝŶŐ​W&dϬϮ​ĂĚŵŝŶŝƐƚƌĂƟŽŶ͕​ǁŚŝĐŚ​ǁĂƐ​ŵĂŶĂŐĞĚ​ǁŝƚŚ​/s​ƐƚĞƌŽŝĚƐ​;ĚĂƚĂ​ŶŽƚ​ƐŚŽǁŶͿ͖​ƉĂƌƟĐŝƉĂŶƚƐ​ϮͲϱ​ƌĞĐĞŝǀĞĚ​ƚŚĞ​ĂĚũƵƐƚĞĚ​ ŝŵŵƵŶŽƐƵƉƉƌĞƐƐŝŽŶ​ƌĞŐŝŵĞŶ Time (days) 0 60 120 180 240 300 36 0 3 6 9 12 15 18 21 24 27 30 33 360 CSF PGRN, ng/mL ParƟcipant 1 ParƟcipant 2 ParƟcipant 3 ParƟcipant 4 ParƟcipant 5 0 20 40 60 80 100 120 140 160 180 200 Screening Day 1 Dosing Day 7 Unsch. Day 13 Unsch. Day 16 Day 30 Day 42 Unsch. Day 53 Unsch. Day 55 Unsch. Day 64 Unsch. Day 71 Unsch. Day 78 Day 90 Day 120 Day 180 Day 240 Day 300 Day 360 ALT (U/L) ALT (U/L) 0 10 20 30 40 50 60 70 80 90 100 Screening Day 1 Dosing Day 7 Unsch. Day 13 Unsch. Day 16 Day 30 Day 42 Unsch. Day 53 Unsch. Day 64 Unsch. Day 78 Day 90 Day 120 Day 180 Day 240 Day 300 Day 360 AST (U/L) AST (U/L) Participant 2 Participant 3 Participant 4 Participant 5 Participant 2 Participant 3 Participant 4 Participant 5 PBFT02 PBFT02 ITR ITR CB7 promoter Chimeric intron Codon ŽƉƟŵŝnjĞĚ​ŚGRN PolyA &ŝŐƵƌĞ​ϭ​ʹ​​W&dϬϮ​ǀĞĐƚŽƌ​ƐƚƌƵĐƚƵƌĞ &ŝŐƵƌĞ​ϰ​W'ZE​ůĞǀĞůƐ​ŝŶ​&​ĨŽůůŽǁŝŶŐ​W&dϬϮ​ ĂĚŵŝŶŝƐƚƌĂƟŽŶ DĞĚŝĐĂů​ǁƌŝƟŶŐ​ƐƵƉƉŽƌƚ​ǁĂƐ​ƉƌŽǀŝĚĞĚ​ďLJ​ WĂƌĞdžĞů​/ŶƚĞƌŶĂƟŽŶĂů​ĂŶĚ​ĨƵŶĚĞĚ​ďLJ​WĂƐƐĂŐĞ​ŝŽ͕​/ŶĐ​ • ƚƵĚŝĞƐ​ŝŶ​ŶŽŶͲŚƵŵĂŶ​ƉƌŝŵĂƚĞƐ​ŚĂǀĞ​ ĚĞŵŽŶƐƚƌĂƚĞĚ​ǁŝĚĞƐƉƌĞĂĚ​ĚŝƐƚƌŝďƵƟŽŶ​ŽĨ​ W&dϬϮ​ƚŚƌŽƵŐŚŽƵƚ​ƚŚĞ​ďƌĂŝŶ​ǁŚĞŶ​ĂĚŵŝŶŝƐƚĞƌĞĚ​ ŝŶƚƌĂƚŚĞĐĂůůLJ​ŝŶ​ƚŚĞ​ĐŝƐƚĞƌŶĂ​ŵĂŐŶĂϭ • /Ŷ​ŵƵƌŝŶĞ​ŵŽĚĞůƐ​ŽĨ​&d͕​ĂĚŵŝŶŝƐƚƌĂƟŽŶ​ŽĨ​ W&dϬϮ​ƌĞƐƚŽƌĞƐ​ůLJƐŽƐŽŵĂů​ĨƵŶĐƟŽŶ​ĂŶĚ​ƌĞĚƵĐĞƐ​ ŶĞƵƌŽĚĞŐĞŶĞƌĂƟŽŶϭ • W&dϬϮ​ŝƐ​ďĞŝŶŐ​ĚĞǀĞůŽƉĞĚ​ĂƐ​Ă​ĚŝƐĞĂƐĞͲŵŽĚŝĨLJŝŶŐ​ ƚŚĞƌĂƉLJ​ĨŽƌ​ŝŶĚŝǀŝĚƵĂůƐ​ǁŝƚŚ​&dͲGRN and &dͲC9orf72 • ,ĞƌĞ​ǁĞ​ƉƌĞƐĞŶƚ​ŝŶƚĞƌŝŵ​ƐĂĨĞƚLJ​ĂŶĚ​ďŝŽŵĂƌŬĞƌ​ ĚĂƚĂ​ĨƌŽŵ​&dͲGRN​ƉĂƌƟĐŝƉĂŶƚƐ​ŝŶ​ƵƉůŝ&dͲ​ ŽŚŽƌƚ​ϭ Methods ƚƵĚLJ​ĚĞƐŝŐŶ • W&dϬϮ​ŝƐ​ďĞŝŶŐ​ĂƐƐĞƐƐĞĚ​ŝŶ​Ă​ƉŚĂƐĞ​ϭͬϮ​ ĐůŝŶŝĐĂů​ƚƌŝĂů​ŝŶ​ƉĂƌƟĐŝƉĂŶƚƐ​ǁŝƚŚ​&dͲGRN and &dͲC9orf72​;ƵƉůŝ&dͲ͖​EdϬϰϳϰϳϰϯϭͿ​;&ŝŐƵƌĞ​ϮͿ • dŚŝƐ​ŵƵůƟͲĐĞŶƚĞƌ͕​ŽƉĞŶͲůĂďĞů͕​ĮƌƐƚͲŝŶͲŚƵŵĂŶ​ƐƚƵĚLJ​ ǁĂƐ​ĚĞƐŝŐŶĞĚ​ƚŽ​ĞǀĂůƵĂƚĞ​ƐĂĨĞƚLJ͕​ƚŽůĞƌĂďŝůŝƚLJ͕​ĂŶĚ​ ƉŚĂƌŵĂĐŽĚLJŶĂŵŝĐƐ​ŽĨ​W&dϬϮ • ĚĚŝƟŽŶĂů​ĞŶĚƉŽŝŶƚƐ​ŝŶĐůƵĚĞ͕​ďŝŽŵĂƌŬĞƌƐ​ŽĨ​ ůLJƐŽƐŽŵĂů​ĚLJƐĨƵŶĐƟŽŶ​ĂŶĚ​ŶĞƵƌŽĚĞŐĞŶĞƌĂƟŽŶ͕​ ŝŵŵƵŶŽŐĞŶŝĐŝƚLJ͕​ĂŶĚ​ĐůŝŶŝĐĂů​ƐƚĂƚƵƐ • W&dϬϮ​ŝƐ​ĂĚŵŝŶŝƐƚĞƌĞĚ​ǀŝĂ​/D​ŝŶũĞĐƟŽŶ​ƵŶĚĞƌ​ d​ŐƵŝĚĂŶĐĞ &ŝŐƵƌĞ​Ϯ​ƵƉůŝ&dͲ​ƐƚƵĚLJ​ĚĞƐŝŐŶ FTD-GRN COHORT 2 Dose 1 (3.3e10 GC/g*) COHORT 3 ;KƉƟŽŶĂůͿ COHORT 4 COHORT 5 FTD-C9orf72 COHORT 1 Dose 1 (3.3e10 GC/g*) Completed IDMC review Ύ'ͬŐ͕​ŐĞŶĞ​ĐŽƉŝĞƐ​ƉĞƌ​ŐƌĂŵ​ŽĨ​ĞƐƟŵĂƚĞĚ​ďƌĂŝŶ​ǁĞŝŐŚƚ ĂƐŚĞĚ​ůŝŶĞƐ​ƌĞƉƌĞƐĞŶƚ​ŽďƐĞƌǀĞĚ​ƌĂŶŐĞ​ŽĨ​W'ZE​ůĞǀĞůƐ​ŝŶ​&​ĨƌŽŵ​ŚĞĂůƚŚLJ​ĂĚƵůƚƐ​ ;ϯ͘Ϯϴʹϴ͘ϭϱ​ŶŐͬŵ>͕​ŶсϲϭͿ ƚƵĚLJ​ƐƚĂƚƵƐ • &ŝǀĞ​ƉĂƌƟĐŝƉĂŶƚƐ​ǁĞƌĞ​ĞŶƌŽůůĞĚ​ŝŶ​ŽŚŽƌƚ​ϭ͖​ ĨŽƵƌ​ƉĂƌƟĐŝƉĂŶƚƐ​ƌĞŵĂŝŶ​ŝŶ​ƚŚĞ​ƐƚƵĚLJ​ĂƐ​ŽĨ​ ƵŐƵƐƚ​ϮϬ͕​ϮϬϮϰ​;ŵŽƐƚ​ƌĞĐĞŶƚ​ĚĂƚĂ​ĐƵƚͿ • KŶĞ​ƉĂƌƟĐŝƉĂŶƚ​ǁŝƚŚĚƌĞǁ​ĨƌŽŵ​ƚŚĞ​ƐƚƵĚLJ​ ϯ​ŵŽŶƚŚƐ​ƉŽƐƚͲW&dϬϮ​ĂĚŵŝŶŝƐƚƌĂƟŽŶ • ŽŚŽƌƚ​Ϯ​ŝƐ​ĐƵƌƌĞŶƚůLJ​ĞŶƌŽůůŝŶŐ • ŽŚŽƌƚ​ϰ​ŝƐ​ĂŶƟĐŝƉĂƚĞĚ​ƚŽ​ďĞ​ŽƉĞŶ​ĨŽƌ​ĞŶƌŽůůŵĞŶƚ​ ŝŶ​ƚŚĞ​ĮƌƐƚ​ŚĂůĨ​ŽĨ​ϮϬϮϱ ZĞĨĞƌĞŶĐĞ͗​ϭ͗​ĂƚĂ​ŽŶ​ĨŝůĞ /ŵŵƵŶŽŐĞŶŝĐŝƚLJ • EŽŶĞ​ŽĨ​ƚŚĞ​ƉĂƌƟĐŝƉĂŶƚƐ​ŝŶ​ŽŚŽƌƚ​ϭ​ŚĂĚ​ĂŶƟͲsϭ​ŶĞƵƚƌĂůŝnjŝŶŐ​ĂŶƟďŽĚŝĞƐ​Ăƚ​ďĂƐĞůŝŶĞ͖​ ĂƐ​ĞdžƉĞĐƚĞĚ͕​Ăůů​ƉĂƌƟĐŝƉĂŶƚƐ​ĚĞǀĞůŽƉĞĚ​ĂŶƟͲsϭ​ĂŶƟďŽĚŝĞƐ​ŝŶ​&​ĂŶĚ​ƐĞƌƵŵ​Ăƚ​ ϯϬ​ĚĂLJƐ​ƉŽƐƚͲW&dϬϮ​ƚƌĞĂƚŵĞŶƚ​ • dǁŽ​ƉĂƌƟĐŝƉĂŶƚƐ​ĚĞǀĞůŽƉĞĚ​dͲĐĞůů​ƌĞƐƉŽŶƐĞ​ĂŐĂŝŶƐƚ​sϭ​ϭϴϬ​ĚĂLJƐ​ƉŽƐƚͲW&dϬϮ​ ƚƌĞĂƚŵĞŶƚ͕​ǁŝƚŚ​ŶŽ​ĐůŝŶŝĐĂů​ƐŝŐŶŝĮĐĂŶĐĞ • EŽ​dͲ​Žƌ​ͲĐĞůů​ŝŵŵƵŶĞ​ƌĞƐƉŽŶƐĞ​ĂŐĂŝŶƐƚ​ŚW'ZE​ǁĂƐ​ĚĞƚĞĐƚĞĚ ​ƐŝŶŐůĞ​ĚŽƐĞ​ŽĨ​W&dϬϮ​ƉƌŽŵŽƚĞƐ​Ă​ƌŽďƵƐƚ​ĂŶĚ​ ĚƵƌĂďůĞ​ŝŶĐƌĞĂƐĞ​ŝŶ​W'ZE​ĞdžƉƌĞƐƐŝŽŶ • ZĞůĂƟǀĞ​ƚŽ​ďĂƐĞůŝŶĞ͕​W&dϬϮ​ŝŶĐƌĞĂƐĞĚ​&​W'ZE​ ĞdžƉƌĞƐƐŝŽŶ​ŝŶ​Ăůů​ƉĂƌƟĐŝƉĂŶƚƐ͖​ƵƉ​ƚŽ​ϲͲĨŽůĚ​Ăƚ​ĚĂLJ​ϯϬ​ ;ŶсϱͿ​ĂŶĚ​ƵƉ​ƚŽ​ϭϬͲĨŽůĚ​Ăƚ​ĚĂLJ​ϭϴϬ​;ŶсϮͿ͘​dŚĞ​ĞīĞĐƚ​ŽĨ​ W&dϬϮ​ǁĂƐ​ĐŽŶƐŝƐƚĞŶƚ​ĂĐƌŽƐƐ​Ăůů​ƉĂƌƟĐŝƉĂŶƚƐ​;&ŝŐƵƌĞ​ϰͿ • &​W'ZE​ůĞǀĞůƐ​ƌĞŵĂŝŶĞĚ​ĞůĞǀĂƚĞĚ​Ăƚ​ĚĂLJ​ϯϲϬ​;ŶсϭͿ͘​ dŚĞ​ƌĂƚĞ​ŽĨ​ŝŶĐƌĞĂƐĞ​ƐůŽǁĞĚ​ďĞƚǁĞĞŶ​ĚĂLJƐ​ϭϴϬ​ĂŶĚ​ϯϲϬ​ ;ϯϬͲϭϴϬ͗​ϱϴй​ǀƐ͘​ϭϴϬͲϯϲϬ͗​ϮϲйͿ • &ŽůůŽǁŝŶŐ​W&dϬϮ​ƚƌĞĂƚŵĞŶƚ͕​ƉůĂƐŵĂ​W'ZE​ĞdžƉƌĞƐƐŝŽŶ​ ƌĞŵĂŝŶĞĚ​ďĞůŽǁ​ƚŚĞ​ƌĂŶŐĞ​ŽďƐĞƌǀĞĚ​ŝŶ​ŚĞĂůƚŚLJ​ĂĚƵůƚƐ​ ĂŵŽŶŐ​Ăůů​ŽŚŽƌƚ​ϭ​ƉĂƌƟĐŝƉĂŶƚƐ​ &ŝŐƵƌĞ​ϯ ,ĞƉĂƚŽƚŽdžŝĐŝƚLJ​ŵĂƌŬĞƌƐ​ƉŽƐƚͲW&dϬϮ​ĂĚŵŝŶŝƐƚƌĂƟŽŶ​ŝŶ​ŽŚŽƌƚ​ϭ​ƉĂƌƟĐŝƉĂŶƚƐ​ ǁŚŽ​ƌĞĐĞŝǀĞĚ​Ă​ƌĞǀŝƐĞĚ​ŝŵŵƵŶŽƐƵƉƉƌĞƐƐŝŽŶ​ƌĞŐŝŵĞŶ​ ĂƐĞůŝŶĞ​ĚĞŵŽŐƌĂƉŚŝĐƐ​ĂŶĚ​ĐůŝŶŝĐĂů​ĐŚĂƌĂĐƚĞƌŝƐƟĐƐ • ĂƐĞůŝŶĞ​ĚĞŵŽŐƌĂƉŚŝĐƐ​ĂŶĚ​ĐůŝŶŝĐĂů​ĐŚĂƌĂĐƚĞƌŝƐƟĐƐ​ŽĨ​ŽŚŽƌƚ​ϭ​ƉĂƌƟĐŝƉĂŶƚƐ​ĂƌĞ​ƐŚŽǁŶ​ in Table 1 • ůů​ƉĂƌƟĐŝƉĂŶƚƐ​ŚĂĚ​Ă​ĐŽŶĮƌŵĞĚ​ƉĂƚŚŽŐĞŶŝĐ​GRN​ŵƵƚĂƟŽŶ​ĂŶĚ​ƐLJŵƉƚŽŵĂƟĐ​&dͲGRN ;Z͕​Ƶŵ​ŽĨ​ŽdžĞƐ​ƐĐŽƌĞƐ​ƌĂŶŐĞĚ​ďĞƚǁĞĞŶ​ϳ​ĂŶĚ​ϭϳͿ ĂLJ​ϭ ĂLJ​ϯϬ ĂLJ​ϲϬ​ ĂLJ​ϭϴϬ ĂLJ​ϯϲϬ Wϭ ϭ͘ϵ ϭϮ͘ϳ Eͬ Eͬ Eͬ WϮ Ϯ͘ϴ ϭϳ͘ϯ Eͬ Ϯϳ͘ϯ ϯϰ͘Ϭ Wϯ Ϯ͘ϵ ϭϬ͘ϳ ϭϯ͘ϳ Ϯϭ͘ϳ Eͬ Wϰ Ϯ͘Ϯ ϭϮ͘ϯ Eͬ Eͬ Eͬ Wϱ Ϯ͘ϯ ϭϯ͘ϲ Eͬ Eͬ Eͬ Table 2 ĚǀĞƌƐĞ​ĞǀĞŶƚƐ​ƌĞƉŽƌƚĞĚ​ĂŵŽŶŐ​ŽŚŽƌƚ​ϭ​ƉĂƌƟĐŝƉĂŶƚƐ ŽŚŽƌƚ​ϭ​;EсϱͿ͕​Ŷ​;йͿ​΀ĞǀĞŶƚƐ΁ ŶLJ​ƚƌĞĂƚŵĞŶƚͲƌĞůĂƚĞĚ​d ϱ​;ϭϬϬ͘ϬͿ​΀ϰϬ΁ DŝůĚ​;'ƌĂĚĞ​ϭͿ ϱ​;ϭϬϬ͘ϬͿ​΀Ϯϵ΁ DŽĚĞƌĂƚĞ​;'ƌĂĚĞ​ϮͿ ϰ​;ϴϬ͘ϬͿ​΀ϵ΁ ĞǀĞƌĞ​;'ƌĂĚĞ​ϯͿ ϭ​;ϮϬ͘ϬͿ΀Ϯ΁ >ŝĨĞ​ƚŚƌĞĂƚĞŶŝŶŐ​;'ƌĂĚĞ​ϰͿ Ϭ​ ĞĂƚŚ​;'ƌĂĚĞ​ϱͿ Ϭ ŶLJ​ ϭ​;ϮϬ͘ϬͿ​΀Ϯ΁ ŶLJ​ƚƌĞĂƚŵĞŶƚͲƌĞůĂƚĞĚ​ ϭ​;ϮϬ͘ϬͿ​΀Ϯ΁ ŶLJ​d​ůĞĂĚŝŶŐ​ƚŽ​ĞĂƌůLJ​ĚŝƐĐŽŶƟŶƵĂƟŽŶ ϭ​;ϮϬ͘ϬͿ DŽƐƚ​ĐŽŵŵŽŶ​d​ďLJ​K​ĂŵŽŶŐ​ŽŚŽƌƚ​ϭ​ƉĂƌƟĐŝƉĂŶƚƐ​ǁĂƐ​ŶĞƌǀŽƵƐ​ƐLJƐƚĞŵ​ĚŝƐŽƌĚĞƌƐ​;Ŷсϰ͖​ϴϬ͘ϬйͿ͘​Ɛ​ŝŶĐůƵĚĞĚ​ŚĞƉĂƚŽƚŽdžŝĐŝƚLJ​ ĂŶĚ​ĐĞƌĞďƌĂů​ǀĞŶŽƵƐ​ƐŝŶƵƐ​ƚŚƌŽŵďŽƐŝƐ​;ĂƐLJŵƉƚŽŵĂƟĐ​ĂŶĚ​ĚĞƚĞĐƚĞĚ​ŽŶ​ĂŶ​ƵŶƐĐŚĞĚƵůĞĚ​DZ/​ƐĐĂŶ​ϱϱ​ĚĂLJƐ​ƉŽƐƚͲƚƌĞĂƚŵĞŶƚͿ͖​ďŽƚŚ​ǁĞƌĞ​ ĐŽŶƐŝĚĞƌĞĚ​ƚƌĞĂƚŵĞŶƚͲ​Žƌ​ƉƌŽĐĞĚƵƌĞͲƌĞůĂƚĞĚ Table 1 ĂƐĞůŝŶĞ​ĚĞŵŽŐƌĂƉŚŝĐƐ​ĂŶĚ​ĐůŝŶŝĐĂů​ĐŚĂƌĂĐƚĞƌŝƐƟĐƐ​ŽĨ​ŽŚŽƌƚ​ϭ​ƉĂƌƟĐŝƉĂŶƚƐ P1 P2 Wϯ Wϰ P5 ŐĞ​;LJĞĂƌƐͿ ϱϭ ϱϵ ϲϬ ϲϵ ϳϭ 'ĞŶĚĞƌ Male &ĞŵĂůĞ Male Male &ĞŵĂůĞ &dͲGRN​ƉŚĞŶŽƚLJƉĞ ůǀWW ďǀ&d ďǀ&d ƐǀWW ďǀ&d ŐĞ​Ăƚ​ĚŝĂŐŶŽƐŝƐ​;ĚŝƐĞĂƐĞ​ĚƵƌĂƟŽŶ͕​LJĞĂƌƐͿ ϰϳ​;ϰͿ ϱϲ​;ϯͿ ϱϵ​;ϭͿ ϲϴ​;ϭͿ ϲϳ​;ϰͿ W'ZE​Ăƚ​ƐĐƌĞĞŶŝŶŐ͕​ƉůĂƐŵĂ​;ŶŐͬŵ>Ϳ ϲϬ͘ϵ ϰϰ͘ϴ ϯϲ͘Ϭ Ϯϱ͘ϱ ϭϳ͘ϰ W'ZE​Ăƚ​ďĂƐĞůŝŶĞ͕​&​;ŶŐͬŵ>Ϳ ϭ͘ϵ Ϯ͘ϴ Ϯ͘ϵ Ϯ͘Ϯ Ϯ͘ϯ ůŝŶŝĐĂů​ĞŵĞŶƟĂ​ZĂƟŶŐ​ĐĂůĞ͕​'ůŽďĂů ϭ Ϯ Ϯ Ϯ ϭ ůŝŶŝĐĂů​ĞŵĞŶƟĂ​ZĂƟŶŐ​ĐĂůĞ͕​Ƶŵ​ŽĨ​ŽdžĞƐ ϳ͘ϱ ϭϳ ϭϮ ϭϭ ϳ ůŝŶŝĐĂů​ĞŵĞŶƟĂ​ZĂƟŶŐ​ĐĂůĞ͕​Ƶŵ​ŽĨ​ŽdžĞƐ​ŚĂƐ​Ă​ƚŽƚĂů​ƐĐŽƌĞ​ŽĨ​Ϯϰ͖​ŚŝŐŚĞƌ​ƐĐŽƌĞƐ​ĂƌĞ​ŝŶĚŝĐĂƟǀĞ​ŽĨ​ŵŽƌĞ​ƐĞǀĞƌĞ​ĚĞŵĞŶƟĂ​ƉŚĞŶŽƚLJƉĞƐ Poster No. 007 ŽƉŝĞƐ​ŽĨ​ƚŚŝƐ​ƉŽƐƚĞƌ​ƉƌĞƐĞŶƚĂƚŝŽŶ​ŽďƚĂŝŶĞĚ​ƚŚƌŽƵŐŚ​YƵŝĐŬ​ZĞƐƉŽŶƐĞ​ ;YZͿ​ŽĚĞ​ĂƌĞ​ĨŽƌ​ƉĞƌƐŽŶĂů​ƵƐĞ​ŽŶůLJ​ĂŶĚ​ŵĂLJ​ŶŽƚ​ďĞ​ƌĞƉƌŽĚƵĐĞĚ​ ǁŝƚŚŽƵƚ​ƉĞƌŵŝƐƐŝŽŶ​ŽĨ​WĂƐƐĂŐĞ​ŝŽ͕​/ŶĐ͘ ŚƚƚƉƐ͗ͬͬďŝƚ͘ůLJͬϯyŬsďϴŚ